The causative agent for AIDS is known to be a virus of the retrovirus family called HIV (human immunodeficiency virus). Infection with HIV does not, however, immediately give rise to overt symptoms of AIDS. The only indication of exposure to the virus may be the presence of antibodies thereto in the blood of an infected subject who is then described as `HIV positive`. The infection may lie dormant, giving rise to no obvious symptoms, and the incubation period prior to development of AIDS may vary from several months to decades. Development of AIDS itself may be preceded by the AIDS-related complex (ARC) which is characterised by unexplained fever, weight loss, chronic cough or diarrhoea.
The reasons for the variable period between infection with the virus and breakdown of the immune system in an infected individual are poorly understood. Factors at present unknown may trigger proliferation of the virus with consequential disruption of the immune system. The victims of the disease are then subject to various infections and malignancies which, unchecked by the disabled immune system, lead to death.
Despite the rapid growth of research into AIDS no vaccine against it is yet available. It has been suggested that the genetic variability of the virus will in fact hamper the search for an effective vaccine.
The association between HIV infection and tuberculosis is well known. An early effect of HIV infection is the reactivation of previously dormant tubercule bacilli. The maintenance of resistance to mycobacteria is an active immunological process which is compromised by HIV infection. In dually infected persons, there is a high reactivation rate of dormant tubercule bacilli and this reactivation usually occurs well before the appearance of other HIV/AIDS-related infections which strongly suggests that an important effect of HIV infection is to destroy precisely those immune functions, presumably T-cell mediated, that maintain mycobacterial dormancy.
There is also evidence that where active tuberculosis is superimposed on HIV infection, there is a dramatic loss of CD4 T-cells which results in very rapid development of overt symptoms of AIDS. It appears in fact that immune mediators released in tuberculosis accelerate transactivation of the HIV provirus.
We have previously described the use of antigenic and/or immuno regulatory material derived from Mycobacterium vaccae in the treatment of tuberculosis (see, for example, British Patent No. 2156673 and U.S. Pat. No. 4,724,144).